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I was aware of the study by Drummond and Park,1 and as Dr. Drummond indicated in his letter, his study bears no direct resemblance to ours.2 The aims and methods of both studies were different. Dr. Drummond studied the effect of different preoxygenation techniques on hemoglobin saturation in patients anesthetized with 3–5 mg/kg thiopental. Neuromuscular block was established with 100 mg succinylcholine. Incremental doses of thiopental and succinylcholine were administered to maintain anesthesia and apnea for 3 min. Dr. Drummond then evaluated the changes in hemoglobin saturation over a period of 3 min. The Hewlett Packard ear oximeter used in Dr. Drummond's study1 was not only “clumsy,” as characterized by Dr. Drummond, but also inaccurate (see Douglas et al.3).

Dr. Drummond disagrees on where to put the emphasis on mechanisms underlying the observed hypoxic trend in my report. He suggested that reduction in functional residual capacity has a more important contribution to hemoglobin desaturation than shunting in anesthetized obese patients. I have described the effect of anesthesia on functional residual capacity in my article.2 I still believe that shunting played a significant role in my observations. In reality, as I stated in the Discussion, “reduced functional residual capacity . . . will result in an increase in shunt fraction because of collapse of alveoli.” Further, Gunnarsson et al.4 reported that 87% (39 of 45) of their patients had development of atelectasis and shunting during anesthesia and concluded that “during anesthesia, shunt influenced PaO2 most.” Although the mechanisms underlying my results may be open to disagreement, the lesson is that the risk of desaturation in the immediate postinduction period is much greater than most clinicians recognize if there were failure to intubate and ventilate our patients.

Dr. Drummond also stated that the model prediction of Hardman et al.5 … was more complete than the model studies” cited in my report. I do not agree. I cited the work of Hardman et al.
Nevertheless, in the study of Hardman et al.
, the authors used a simulator to examine the onset and course of hypoxemia during apnea. They evaluated one factor at a time (and this does not reflect the clinical reality). They concluded that the time to 50% oxyhemglobin saturation varied from 11 to 8 min in an open and an obstructed airway apneic patient model, respectively. This prediction is at variance with my observations2 and those of others.6 Although none of patients in my study2 or the volunteers in the study of Heier et al.6 were allowed to have hemoglobin saturation decreased less than 90% and less than 80%, respectively, times to 50% hemoglobin saturation in the aforementioned studies would have been shorter than that predicted by Hardman et al.5

Models, by definition, attempt to simplify reality. Models can be useful and effective teaching tools, but ultimately, they require validation. The observations in my investigation were much more alarming than conventional wisdom (and modeling) would predict. When observed data conflicts with theory, it is the theory that must be challenged.